The contractile status of a muscle can be assessed by measuring the force-length relationship, or pressure-volume relationship in the case of cardiac muscle. Generally, measurement of this relationship requires instantaneous measurements of force and length, or pressure and volume, simultaneously. The contractile status of cardiac muscle can be computed as the instantaneous stiffness, E(t), which is the ratio of the instantaneous developed pressure P(t) to the associated change in ventricular volume (V(t)-V0). The contractile status of skeletal muscle can be computed as the instantaneous stiffness, K(t), equal to the ratio the instantaneous developed force F(t) to the associated change in length (L(t)-L0). These ratios are related to the calcium cycling of the muscle fibers and formation of strong bonds between myofilaments.
Obtaining instantaneous force and length or pressure and volume measurements directly is generally an invasive procedure that is not technically convenient or easily performed. As such, measurements for assessing the contractile status of skeletal muscle, the heart or other muscular organ are not widely used in clinical diagnosis, monitoring of a medical condition, or managing medical treatment. Information regarding the contractility or inotropic state of a muscle would be valuable to a clinician in managing medical treatment.
In general, contractility refers to the amount of force or pressure a muscle generates at a given resting length or preload. Changes in contractility reflect changes in the inotropic state of the muscle. The inotropic state can be altered by disease. Hemodynamic performance of the heart depends on the preload (the ventricular end-diastolic fiber length), the afterload, and the inotropic state of the myocardium. Hemodynamic evaluation often includes measurements of ejection fraction, stroke volume, and systolic and diastolic pressures and volumes which are affected by changes in ventricular contractility but are also influenced by changes in preload and afterload. Such measures therefore do not provide an assessment of ventricular contractility independent of influences of afterload and preload. Indices of myocardial function can be derived from methods such as obtaining pressure-volume loops and determining end-systolic pressure-volume relationships or preload recruitable stroke work. However, these methods are complicated, time-consuming and require considerable skill.